瘦素在中枢神经系统髓鞘再生中的作用

K. Matoba, R. Muramatsu, T. Yamashita
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引用次数: 0

摘要

瘦素是一种小鼠肥胖基因,在人类中也存在。相对于其他组织,瘦素受体在下丘脑高度表达;因此,瘦素的功能主要归因于下丘脑对食物摄入和体重的控制。虽然瘦素受体的表达并不局限于下丘脑,也存在于中枢神经系统(CNS)的其他区域,如脊髓,但瘦素和瘦素受体在中枢神经系统(CNS)中的功能尚未完全阐明。在本研究重点中,我们重点关注瘦素在病理条件下,如脱髓鞘小鼠模型中,在中枢神经系统脱髓鞘中的新功能。由于髓鞘再生是损伤和伤口愈合后神经网络修复的关键过程,因此了解髓鞘再生的潜在分子机制有助于建立针对脱髓鞘疾病的治疗策略。我们只在组织学水平上揭示了瘦素在髓鞘再生中的作用;然而,对瘦素对人类有益作用的行为分析和证据可能会增加对瘦素对髓鞘再生功能影响的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of leptin in the central nervous system remyelination
Leptin is identified as a mouse obesity gene, which is also preserved in humans. Leptin receptor is highly expressed in the hypothalamus relative to other tissues; therefore, the function of leptin is mainly attributed to hypothalamic control of food intake and body weight. Although the expression of leptin receptors is not limited to the hypothalamus but is also present in other regions of the central nervous system (CNS), such as the spinal cord, the functions of leptin and leptin receptor in the CNS have not been fully clarified. In this research highlight, we focus on the novel function of leptin in CNS remyelination in pathologic conditions, such as the demyelination mouse model. Because remyelination is a crucial process for repair of neuronal networks after injury and wound healing, knowledge of the underlying molecular mechanism of remyelination is useful to establish a therapeutic strategy against demyelinating diseases. We only revealed the role of leptin in remyelination at a histological level; however, a behavioral analysis and evidence of the beneficial effect of leptin for humans may add to knowledge of the effect of leptin on remyelination function.
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